Pathophysiology
Acne vulgaris is a disease of the sebaceous glands. The condition is associated with sebaceous hypersecretion and is dependent on the sexual hormones testosterone and sex hormone-binding globulin (SHBG) (2). Abnormal cornification of the pilosebaceous canal is caused by increased proliferation or reduced shedding of keratinocytes, which cause the formation of a plug of sebum and keratin. The anaerobic, Gram positive microorganism Propionibacterium acnes proliferates in the anaerobic, lipid-rich environment caused by the increased production of sebum. A high production of sebum results in a higher concentration of P. acnes, although there is no correlation between the number of bacteria on the skin surface and the severity of the acne.
P. acnes produces lipases, which, in combination with other biologically active substances, decompose sebum, thereby releasing fatty acids and hydrolytic enzymes. These affect the sebaceous glands and stimulate an inflammatory response, with a preponderance of the cytokines IL-1-α, IL-β and TNF. Studies indicate that acne is a primary inflammatory disease, since upregulated CD3-positive and CD4-positive T-cells have been found in microcomedones, as well as an increased number of macrophages and upregulated inflammatory vascular markers prior to hyperkeratinization and hyperplasia of the sebaceous glands (3).
The impact of nutrition on the development of acne has been widely debated. Several recent studies indicate that intake of foods rich in quickly degradable carbohydrates causes hyperglycemia, which stimulates the secretion of insulin and the release of an insulin-like growth factor (IGF-1). IGF-1 has a direct effect on the sebaceous glands and stimulates epidermal hyperplasia, which increases the risk of development of acne (4).
Other potentially aggravating factors include sweating, smoking and stress. Some patients experience deterioration in the pre-menstrual period and in times of increased air humidity, while sunlight often improves the condition (5, 6).